Regulation and Integration of the Body
hormones, glucocorticoids act on target cells by modifying gene
Negative feedback regulates glucocorticoid secretion. Cor-
tisol release is promoted by ACTH. ACTH release is triggered
in turn by the hypothalamic releasing hormone CRH. Rising
cortisol levels feed back to act on both the hypothalamus and
the anterior pituitary, preventing CRH release and shutting off
ACTH and cortisol secretion.
Cortisol secretory bursts, driven by patterns of eating and ac-
tivity, occur in a definite pattern throughout the day and night.
Cortisol blood levels peak shortly before we rise in the morning.
±e lowest levels occur in the evening just before and shortly af-
ter we fall asleep. However, acute stress of any variety interrupts
the normal cortisol rhythm as higher CNS centers override the
(usually) inhibitory effects of elevated cortisol levels and trig-
ger CRH release. ±e resulting increase in ACTH blood levels
causes an outpouring of cortisol from the adrenal cortex.
Stress results in a dramatic rise in blood levels of glucose,
fatty acids, and amino acids, all provoked by cortisol. Cortisol’s
prime metabolic effect is to provoke
, that is, the
formation of glucose from fats and proteins. In order to “save”
glucose for the brain, cortisol mobilizes fatty acids from adipose
tissue and encourages their increased use for energy. Under
cortisol’s influence, stored proteins are broken down to provide
building blocks for repair or to make enzymes for metabolic
processes. Cortisol enhances the sympathetic nervous system’s
vasoconstrictive effects, and the rise in blood pressure and cir-
culatory efficiency that results helps ensure that these nutrients
are quickly distributed to cells.
Note that
ideal amounts of glucocorticoids promote normal func-
, but too much cortisol exerts significant anti-inflammatory
and anti-immune effects. Excessive levels of glucocorticoids
Depress cartilage and bone formation
Inhibit inflammation by decreasing the release of inflamma-
tory chemicals
Depress the immune system
Disrupt normal cardiovascular, neural, and gastrointestinal
Glucocorticoid drugs can control symptoms of many chronic
inflammatory disorders, such as rheumatoid arthritis and aller-
gic responses. However, these potent drugs are a double-edged
sword because they also cause the undesirable effects of exces-
sive levels of these hormones.
Homeostatic Imbalance
±e pathology of glucocorticoid excess,
Cushing’s syndrome
may be caused by an ACTH-releasing pituitary tumor (in which
case it is called
Cushing’s disease
); by an ACTH-releasing ma-
lignancy of the lungs, pancreas, or kidneys; or by a tumor of the
adrenal cortex. However, it most oFen results from the clinical
administration of glucocorticoid drugs.
±e syndrome is characterized by persistent elevated blood
glucose levels (
steroid diabetes
), dramatic losses in muscle and
bone protein, and water and salt retention, leading to hyperten-
sion and edema. ±e so-called
cushingoid signs
(Figure 16.16)
When blood pressure (or blood volume) falls, specialized cells
of the
juxtaglomerular complex
in the kidneys are excited.
±ese cells respond by releasing
into the blood.
Renin cleaves off part of the plasma protein
sin-o-jen), triggering an enzymatic
cascade that forms
angiotensin II
, which stimulates the
glomerulosa cells to release aldosterone.
However, the renin-angiotensin-aldosterone mechanism
does much more than trigger aldosterone release, and all of its
effects ultimately raise blood pressure. We describe these addi-
tional effects in Chapters 19 and 26.
Plasma Concentrations of Potassium
²luctuating blood levels
of K
directly influence the zona glomerulosa cells in the adre-
nal cortex. Increased K
stimulates aldosterone release, whereas
decreased K
inhibits it.
Under normal circumstances, ACTH released by the
anterior pituitary has little or no effect on aldosterone release.
However, when a person is severely stressed, the hypothalamus
secretes more corticotropin-releasing hormone (CRH), and the
resulting rise in ACTH blood levels steps up the rate of aldoste-
rone secretion to a small extent. ±e resulting increase in blood
volume and blood pressure helps deliver nutrients and respira-
tory gases during the stressful period.
Atrial Natriuretic Peptide
Atrial natriuretic peptide, a
hormone secreted by the heart when blood pressure rises, fine-
tunes blood pressure and sodium-water balance of the body.
One of its major effects is to inhibit the renin-angiotensin-
aldosterone mechanism. It blocks renin and aldosterone secre-
tion and inhibits other angiotensin-induced mechanisms that
enhance water and Na
reabsorption. Consequently, ANP’s
overall influence is to decrease blood pressure by allowing Na
(and water) to flow out of the body in urine (
ducing salty urine).
Homeostatic Imbalance
Hypersecretion of aldosterone, a condition called
, typically results from adrenal tumors. Two major
sets of problems result: (1) hypertension and edema due to
excessive Na
and water retention, and (2) accelerated excre-
tion of potassium ions. If K
loss is extreme, neurons become
nonresponsive, leading to muscle weakness and eventually
Essential to life, the
influence the energy metab-
olism of most body cells and help us resist stressors. Under nor-
mal circumstances, they help the body adapt to intermittent food
intake by keeping blood glucose levels fairly constant, and main-
tain blood pressure by increasing the action of vasoconstrictors.
However, severe stress due to hemorrhage, infection, or physical
or emotional trauma evokes a dramatically higher output of glu-
cocorticoids, which helps the body negotiate the crisis.
Glucocorticoid hormones include
cortisol (hydrocorti-
, and
, but only cortisol is se-
creted in significant amounts in humans. As with all steroid
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